title: Possible implication of Fc γ receptor-mediated trogocytosis in susceptibility to systemic autoimmune disease.
abstract: Leukocytes can "gnaw away" the plasma membrane of other cells. This phenomenon, called trogocytosis, occurs subsequent to cell-to-cell adhesion. Currently, two mechanisms of trogocytosis, adhesion molecule-mediated trogocytosis and Fc γ receptor-(Fc γ R-) mediated trogocytosis, have been identified. In our earlier study, we established an in vitro model of Fc γ R-mediated trogocytosis, namely, CD8 translocation model from T cells to neutrophils. By using this model, we demonstrated that the molecules transferred to neutrophils via Fc γ R-mediated trogocytosis were taken into the cytoplasm immediately. This result suggests that the chance of molecules transferred via Fc γ R-mediated trogocytosis to play a role on the cell surface could be time-limited. Thus, we consider the physiological role of Fc γ R-mediated trogocytosis as a means to remove antibodies (Abs) that bind with self-molecules rather than to extract molecules from other cells. This concept means that Fc γ R-mediated trogocytosis can be a defense mechanism to Ab-mediated autoimmune response. Moreover, the activity of Fc γ R-mediated trogocytosis was revealed to be parallel to the endocytotic activity of neutrophils, which was critically related to the susceptibility to systemic autoimmune diseases. The collective findings suggest that Fc γ R-mediated trogocytosis could physiologically play a role in removal of Abs bound to self-antigens and prevent autoimmune diseases.
authors.affiliation: Graduate School of Health Sciences, Hokkaido University, Sapporo 060-0812, Japan.
authors.forename: Sakiko
authors.initials: S
authors.lastname: Masuda
authors.forename: Sari
authors.initials: S
authors.lastname: Iwasaki
authors.forename: Utano
authors.initials: U
authors.lastname: Tomaru
authors.forename: Tomohisa
authors.initials: T
authors.lastname: Baba
authors.forename: Kazuaki
authors.initials: K
authors.lastname: Katsumata
authors.forename: Akihiro
authors.initials: A
authors.lastname: Ishizu
mesh_terms: D001327:Autoimmune Diseases / Q000276:immunology* / Q000378:metabolism*; D004705:Endocytosis; D006801:Humans; D017452:Receptors, IgG / Q000276:immunology / Q000378:metabolism*; D057900:Transcytosis / Q000276:immunology*
chemical_list: D017452:Receptors, IgG